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Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is an autosomal dominant neurodegenerative tauopathy and Parkinson plus syndrome. [3] FTDP-17 is caused by mutations in the MAPT (microtubule associated protein tau) gene located on the q arm of chromosome 17, and has three cardinal features: behavioral and personality changes, cognitive impairment, and motor symptoms.
There are three main histological subtypes found at post-mortem: FTLD-tau, FTLD-TDP, and FTLD-FUS. In rare cases, patients with clinical FTD were found to have changes consistent with Alzheimer's disease on autopsy. [41] The most severe brain atrophy appears to be associated with behavioral variant FTD, and corticobasal degeneration. [42]
Frontotemporal lobar degeneration; Neuropathologic analysis of brain tissue from FTLD-TDP patients. Ubiquitin immunohistochemistry in cases of familial FTLD-TDP demonstrates staining of (a) neurites and neuronal cytoplasmic inclusions in the superficial cerebral neocortex, (b) neuronal cytoplasmic inclusions in hippocampal dentate granule cells, and (c) neuronal intranuclear inclusions in the ...
Primary age-related tauopathy (PART) is a neuropathological designation introduced in 2014 to describe the neurofibrillary tangles (NFT) that are commonly observed in the brains of normally aged and cognitively impaired individuals that can occur independently of the amyloid plaques of Alzheimer's disease (AD).
Alternatively, diseases exhibiting tau pathologies attributed to different and varied underlying causes are termed 'secondary tauopathies'. Some neuropathologic phenotypes involving tau protein are Alzheimer's disease , frontotemporal dementia , progressive supranuclear palsy , and corticobasal degeneration .
However, when tau is hyperphosphorylated, it is unable to bind and the microtubules become unstable and begin disintegrating. The unbound tau clumps together in formations called neurofibrillary tangles. [4] More explicitly, intracellular lesions known as pretangles develop when tau is phosphorylated excessively and on improper amino acid residues.
Gabapentin aims to reduce pain and provide relief by altering the normal functioning of neurotransmitters that induce a sensation of pain and discomfort. [28] However, the exact mechanism of Gabapentin’s functioning in the body is not completely understood and current knowledge is based on experimental studies that target the nervous system. [29]
In other words, the symptoms of LATE are similar to those of Alzheimer's disease. The acronym LATE stands for L imbic-predominant A ge-related T DP-43 E ncephalopathy. “ Limbic ” is related to the brain areas first involved, “age-related” and the name “LATE” itself refer to the onset of disease usually in persons aged 80 or older.